Numerous studies have linked chronic inflammation to the development of BPH but how inflammation leads to cellular proliferation and hyperplasia is unclear. We know that cell-to-cell signaling, as part of repair and recovery during the resolution phase of inflammation, produces a microenvironment rich in factors that promote cellular proliferation and differentiation. Tissue repair secondary to inflammation proceeds by a defined series of events that clears damaged cells, removes cellular debris, directs the proliferation of progenitor cells, and finally, differentiation and tissue repopulation. In chronic inflammation, tissue repair can lose its self-limiting quality, generating hyperplasia. The mechanisms by which the repair process becomes dysregulated are not well defined and represent a significant deficit in our understanding of inflammation and BPH. The impact of inflammation on the adult basal prostate stem cells (bPSC) is largely unclear. This specialized cell population is known to maintain and repair the cellular integrity of the prostate. Previous data from our laboratories showed that inflammation stimulates bPSC expansion and epithelial hyperplasia. Interestingly, bPSC from inflamed prostates generate larger organoids ex vivo than bPSC from non-inflamed mice, indicating that inflammation induces processes that sustain proliferative capacity. Others demonstrated an inflammation-driven bPSC to luminal progenitor transition, supporting the hypothesis that bPSC are linked to luminal epithelial expansion. Given the ability of inflammation to induce bPSC to expand and differentiate into all epithelial cell types of the prostate and the omnipresence of inflammation in BPH specimens, the underlying scientific premise of our work is that inflammation induces adult bPSC expansion that drives epithelial hyperplasia in BPH. Unexpected and novel findings involving inflammation and bPSC show inflammation to stabilize AR in freshly isolated bPSC and cultured organoids. AR nuclear translocation was observed as was AR-mediated transcriptional activity. Notably, AR was essential for human and mouse organoid growth, as AR inhibition with ENZ, AR-specific shRNA knock-down, Abiraterone or Dutasteride abrogated organoid growth. Single cell RNA-seq comparing inflamed and nave bPSC revealed an elevation of autocrine interleukin-1? (IL-1?) and its receptor (IL1R1) in inflamed bPSC (11.4- and 5-fold (log2), respectively). IL1? mRNA induction was verified by qRT-PCR and intracellular protein by immunofluorescence. IL-1 signaling was verified by identification of phosphorylated IRAK in inflamed but not nave bPSC and surprisingly, ENZ significantly down-regulated autocrine IL-1? and IL1R1, while upregulating the IL-1 inhibitor, IL-1ra. IL-1? induction continued in human BPH and murine organoid cultures, indicating sustained production in the absence of inflammatory cells. Critically, IL-1 signaling was shown to be necessary for inflammation- induced bPSC expansion in vivo, for organoid growth ex vivo and it exacerbated basal and luminal hyperplasia in vivo. These novel findings are the basis of our hypothesis that inflammation-induced AR stabilization and IL-1 signaling drive inflammation induced bPSC expansion, leading to basal and luminal hyperplasia.